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52 publications mentioning hsa-mir-187

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-187. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 290
MiR-187 downregulation predicts poor prognosis in clear cell renal cell carcinoma, demonstrating that miR-187 downregulation is associated with higher tumor grade and stage and plays a tumor-suppressive role [17]. [score:9]
An increasing amount of evidence has validated the use of down-regulated and up-regulated miR-187 as a tumor suppressor gene or oncogene, respectively, and miR-187 is closely related with tumor cell proliferation and apoptosis. [score:9]
In this study, microarray analysis detected miR-187 downregulation in CC tissues; subsequently, we measured miR-187 expression in CC tissues and cell lines, and found that miR-187 was significantly downregulated as compared with miR-187 expression in the corresponding normal controls. [score:8]
Deregulated miR-187 expression regulates HPV16 E6 mRNA and p53 protein expression. [score:7]
We transfected CaSki cells with miR-187 inhibitor or miR-187 inhibitor control to demonstrate whether low miR-187 expression contributes to tumor progression. [score:7]
Conversely, 48-h transient transfection with 40 nM miR-187 inhibitor markedly increased the relative expression of HPV16 E6 mRNA and decreased p53 protein expression in the co-cultures (Figure 4D–4F). [score:7]
The results suggest that miR-187 overexpression inhibits CC tumor growth in vivo. [score:5]
To verify this prediction, we detected the expression of HPV16 E6 mRNA in CaSki cells in the presence of miR-187 mimics or miR-187 inhibitor. [score:5]
miR-187 overexpression inhibits tumor growth of CC in vivo. [score:5]
Kaplan–Meier curves revealed higher rates of OS and relapse-free survival of the high miR-187 expression group than in the low miR-187 expression group (Figure 2C). [score:5]
miR-187 mimics, a nonspecific mimic control, miR-187 inhibitor, and a nonspecific inhibitor control were all purchased from GenePharma (Shanghai, China). [score:5]
To elucidate the pattern of miR-187 expression in CC, we first detected miR-187 expression levels in 209 cervical tissue samples using real-time PCR, which included 82 carcinoma tissues and the matched normal tissues (5 cm distal from the tumor), and 45 cervical squamous intraepithelial lesions. [score:5]
Figure 2 (A) Heatmap analysis of the expression of 41 miRNAs in normal cervical tissues and CC tissues, miR-187 expression is low. [score:5]
Figure 5 (A) CCK-8 detection of miR-187 overexpression inhibition of CaSki cell proliferation (*P < 0.05). [score:5]
MiR-187 mimics significantly reduced HPV16 E6 mRNA expression, and miR-187 inhibitor increased it (Figure 8A). [score:5]
miR-187 overexpression inhibits CaSki cell proliferation, migration, and invasion, and promotes CaSki cell apoptosis. [score:5]
Low miR-187 expression was significantly associated with pathological grade, clinical stage, nodal metastasis, and larger tumor size (all, P < 0.05), suggesting that decreased miR-187 expression may be involved in CC progression and metastasis. [score:5]
Twenty-three miRNAs were over-expressed and eighteen miRNAs, including miR-187, were low expression. [score:5]
Furthermore, we found that the rates of OS and relapse-free survival of the high miR-187 expression group were higher than that of the low miR-187 expression group. [score:5]
Most excitingly, we demonstrated that miR-187 acts as a tumor suppressor by targeting HPV 16E6 in CaSki cell proliferation and invasive capacity, and apoptosis. [score:5]
Taken together, these results suggest that miR-187 over -expression inhibits CC tumor growth in vitro. [score:5]
Low miR-187 expression promotes CaSki cell proliferation, migration, and invasion, and inhibits CaSki cell apoptosis. [score:5]
Therefore, our results suggest that miR-187 may play crucial roles in CC development and progression by targeting HPV16 E6. [score:4]
Collectively, these findings indicated that low miR-187 expression correlates with the clinical outcome in CC and might play a role in CC development or progression. [score:4]
MiR-187 overexpression inhibits CaSki cell proliferation, migration, and invasion, and promotes CaSki cell apoptosis. [score:4]
miR-187 knockdown promotes CaSki cell proliferation, migration, and invasion, and inhibits CaSki cell apoptosis. [score:4]
However, further research is still needed to explore whether or how miR-187 can directly target HPV16 E6. [score:4]
Furthermore, we identified HPV16 E6 as a direct and functional target of miR-187. [score:4]
Indeed, we confirmed that HPV 16E6 mRNA and protein were regulated by the high or low expression of miR-187, as showed by Real-time-PCR and, respectively. [score:4]
MiR-187 overexpression suppressed CC cell proliferation, migration, and invasion, and promoted CC cell apoptosis. [score:4]
Cell Counting Kit-8 (CCK-8) showed that the inhibitory rate of cells growth treated with miR-187 mimics was inhibited compared with cells transfected with negative control (NC) mimics (Figure 5A). [score:4]
HPV16 E6 is a direct target of miR-187. [score:4]
In a miRNA–mRNA direct-interaction CLASH (crosslinking, ligation, and sequencing of hybrids) experiment, Helwak et al. [30] found that TUBG1, MAD2L2, and STOML2 were target genes of miR-187. [score:4]
Recent studies have shown significant miR-187 upregulation in many human malignancies. [score:4]
But in pancreatic cancer, low miR-187 expression predicts short overall survival (OS) in patients after radical surgery [15]. [score:3]
We also analyzed the prognostic value of miR-187 expression in patients with CC. [score:3]
However, HPV18 E6 and E7 mRNA expression were unchanged, indicating no association between miR-187 and HPV18 E6/E7. [score:3]
These findings suggested the functions of miR-187 expression patterns may be tissue-specific. [score:3]
As expected, miR-187 suppression significantly promoted CaSki cell proliferation (Figure 7A), migration (Figure 7B), and invasion (Figure 7C). [score:3]
miR-187 expression and age and pathological type were not significantly correlated. [score:3]
MiR-187 is downregulated in CC and correlates with CC prognosis. [score:3]
Taken together, these observations indicate that low miR-187 expression promotes CC tumor progression by negatively controlling these cellular phenotypes. [score:3]
DAB2 [14] and matrix metalloproteinase (MMP) [28] are target genes of miR-187. [score:3]
Ectopic expression of miR-187 has been reported in nasopharyngeal [16], renal [17], pancreatic [18], prostate [19], thyroid [20], gastric [21], and esophageal cancer [22] and in neuroblastoma [23]. [score:3]
There was a significant difference between miR-187 expression and pathological grade, clinical stage, tumor size, and lymph node metastasis (Table 1). [score:3]
These findings indicated that established RT-qPCR methods can detect the corresponding target genes of miR-187. [score:3]
Figure 8 (A) HPV16 E6 mRNA levels detected in the presence of miR-187 mimics or miR-187 inhibitor (**P < 0.01, ***P <0.001). [score:3]
The wound healing assay was conducted to confirm the role of miR-187 in CC progress, and showed that CaSki cells overexpressing miR-187 were less efficient at closing an artificial wound compared to CaSki cells expressing miR-NC (CaSki, 48 h, Figure 5B). [score:3]
The mimics increased miR-187 expression in the cells (Figure 4A). [score:3]
To explore the mechanisms of miR-187 in CC, we identified HPV16 E6 as a putative miR-187 target gene, and selected it for further study. [score:3]
For example, high miR-187 expression in breast cancer leads to a more aggressive, invasive phenotype and acts as an independent predictor of outcome [13]. [score:3]
Figure 7 (A) CCK-8 detection of CaSki cell proliferation promoted by low miR-187 expression (*P < 0.05). [score:3]
miR-187 affects the expression of HPV16 E6 mRNA and p53 protein. [score:3]
The miR-187/HPV16 E6 axis provides novel insight into CC pathogenesis, and it might represent a potential therapeutic target in CC. [score:3]
Figure 4 (A) Detection of miR-187 expression levels after mimics transfection. [score:3]
In ovarian cancer, excessive miR-187 promotes tumor progression through by disabled homolog 2 (DAB2), inhibiting epithelial–mesenchymal transition [14]. [score:3]
In order to explore the mechanisms of miR-187, we identified HPV16 E6 as a putative miR-187 target gene. [score:3]
Also we proved that HPV 16E6 is a direct target of miR-187 by dual luciferase reporter gene assay. [score:3]
Association between miR-187 expression and clinicopathological parameters of CC. [score:3]
miR-187 mimics increased miR-187 levels in the tumor microenvironment and inhibited CaSki cell growth in nude mice (Figure 6A, 6B). [score:3]
Association between miR-187 expression and the clinicopathological parameters of CC. [score:3]
miR-187 expression is low in CC and correlates with prognosis of CC. [score:3]
Based on the results, we discovered a new target gene HPV 16E6 of miR-187, which is an interesting and important topic. [score:3]
A site-directed mutagenesis kit (Beyotime, Jiangsu, China) was used to construct the mutant miR-187 -binding site vector (pmir-GLO-mUTR) according to the manufacturer's protocol. [score:2]
Conversely, miR-187 knockdown significantly facilitated the malignant phenotype of CC cells. [score:2]
In addition to the in vitro experiment, we validated our findings in nude mice, where the tumors formed in nude mice treated with miR-187 mimics were significantly smaller than that of the control group. [score:1]
The reporter vector carrying the partial sequence of the HPV16 E6 3′ UTR was cotransfected with miR-187 mimic in Chinese hamster ovary (CHO) cells. [score:1]
Human HPV16 E6 3′ UTR containing the predicted miR-187 binding site was inserted into the 3′ UTR downstream of the firefly luciferase gene of the pmirGLO vector (pmir-GLO-UTR). [score:1]
CaSki cells (4 × 10 [5]/well) were seeded in 12-well plates and transfected with miR-187 mimics. [score:1]
When the average tumor size was 100 mm [3], the mice were randomly separated into two groups subcutaneously injected with miR-187 mimics or miR-187 NC at different sites. [score:1]
We investigated the potential miR-187 target gene HPV16 E6 to explore the mechanism by which miR-187 affects the biological functions of CaSki cells. [score:1]
The best intervention time is 48 h and 40 nM of miR-187 mimics due to the maximum level of miR-187. [score:1]
Figure 3Intervention times (24 h, 48 h, 72 h) and intervention concentrations (20 nM, 40 nM, 80 nM) of miR-187 in (A) HeLa cells and (B) CaSki cells. [score:1]
Subsequently, we measured miR-187 expression levels in two CC cell lines (HeLa cells and CaSki cells) and in the normal C8 cervical epithelial cell line using real-time RT-PCR (Figure 2D). [score:1]
Similarly, we discovered that miR-187 expression levels are associated with pathological grade, clinical stage, nodal metastasis, and larger tumor size via correlation analysis of the clinicopathological characteristics of CC. [score:1]
Figure 1 (A) Image shows 4% agarose electrophoresis of GAPDH, miR-187, HPV18 E6/E7, HPV16 E6/E7, and U6 PCR products. [score:1]
At the same time, miR-187 transfection had no effect on HPV16 E7, suggesting that miR-187 cannot activate HPV16 E7 in CC or HPV16 E7 might not contain high free energy binding sites of miR-187; perhaps other mechanisms not found in this research are present. [score:1]
Specificity analysis of miR-187. [score:1]
The best miR-187 intervention time and concentration. [score:1]
In the present study, we report significantly decreased miR-187 in CC tissues and cell lines. [score:1]
Consistently, elevated caspase-3/-7 activity was also observed in the miR-187 mimics group (Figure 5D). [score:1]
Intervention times (24 h, 48 h, 72 h) and intervention concentrations (20 nM, 40 nM, 80 nM) of miR-187 in (A) HeLa cells and (B) CaSki cells. [score:1]
Therefore, we focused on the role of miR-187 in HPV16+ CaSki cell and HPV18+ HeLa cell over other HPV subtypes or HPV -negative cells. [score:1]
demonstrated that miR-187 decreased HPV16 E6 protein levels in CaSki cells (Figure 8B), which supported our hypothesis. [score:1]
The best miR-187 treatment duration and concentration was 48 h and 40 nM, respectively (Figure 3A, 3B), where miR-187 levels were highest in the cultures. [score:1]
MiR-187 expression was lower in the CC cells (HeLa cells, HPV18 -positive; CaSki cells, HPV16 -positive) as compared to the C8 cells. [score:1]
Moreover, the relative luciferase activity of the reporter containing wild-type HPV16 E6 3′-UTR was markedly decreased upon miR-187 co-transfection (Figure 8D, P< 0.01), whereas the luciferase activity of the reporter containing the mutant binding site was unaffected. [score:1]
We performed a subcutaneous tumor transplantation experiment to confirm the role of miR-187 in tumor growth (Figure 6A). [score:1]
In summary, the present study describes a novel link between miR-187 and HPV16 E6 in CC. [score:1]
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2
[+] score: 288
Our previous screening study identified miR-187 up-regulation in HNSCC [7], and the present study further confirms the up-regulation of miR-187 in OSCC tissues and correlates miR-187 up-regulation with lymph node metastasis. [score:10]
With modest up-regulation of miR-187 in OSCC, and Western blot unequivocally demonstrated a drastic down-regulation of BARX2 expression in OSCC tumors relative to paired normal mucosa. [score:9]
This decreased expression could be caused by the combined effects of BARX2 deletion and the targeting effects of miR-187, since miR-187 was not greatly up-regulated in cancer cells relative to normal cells. [score:8]
Figure 1Up-regulation of miR-187 expression in OSCC(A, C) Box and whiskers plots illustrating the expression of miR-187 in tumor tissue pairs (A) and plasma (C) detected by. [score:8]
Upon treatment with an miR-187 inhibitor, endogenous and exogenous miR-187 expression was drastically suppressed (Figure 2F). [score:7]
Exogenous miR-187 expression (Figure 3F, left) was associated with decreased BARX2 mRNA expression (Figure 3F, middle) and BARX2 protein expression (Figure 3F, right) in HSC3 cells. [score:7]
miR-187 expression increased OSCC oncogenicityCell subclones expressing miR-187 were established in SAS and OECM1 cells, which have high and low endogenous miR-187 expression, respectively (Figure 2A). [score:7]
A further understanding of the signals that up-regulate miR-187 expression and downstream effectors of BARX2 is needed to clarify the role of this regulatory axis in neoplastic processes. [score:7]
Up-regulation of miR-187 expression in OSCC. [score:6]
We observed that OSCC cell lines exhibited decreased BARX2 expression compared to that of NOK cells, possibly due to allele loss or targeting by endogenously-expressed miR-187 in cancer cells. [score:6]
Increased miR-187 expression in OSCC tumors and patient plasmaTo explore the expression of miR-187, 56 OSCC tumors and their paired NCMTs were subjected to (Table S1). [score:5]
Cell subclones expressing miR-187 were established in SAS and OECM1 cells, which have high and low endogenous miR-187 expression, respectively (Figure 2A). [score:5]
Identification of BARX2 as the target gene of miR-187 in OSCC Dab2 was reported to be a target of miR-187 in ovarian cancers [17]. [score:5]
This study suggests that miR-187 may contribute to OSCC progression through suppression of BARX2 expression and indicates the clinical importance of the miR-187–BARX2 cascade in tumor metastasis. [score:5]
To test the targeting activity of miR-187, fragments of 3′ UTR sequences of BARX2, BCL6, DYRK2, FAM80B, GRIA3, and HIPK3 containing predicted miR-187 target sites were amplified by PCR (Table S3) and cloned into the pCMV-LacZ plasmid [7]. [score:5]
In animals carrying relatively smaller tumors, miR-187 expression significantly increased the neck metastasis, and this increase can be rescued by concordant BARX2 expression (Figure 6C). [score:5]
FIH, a tumor suppressor gene in HNSCC [7], was predicted to be a target of miR-187. [score:5]
Of the potential targets, BARX2 emerged as a target of miR-187, as the reporter activity decreased significantly, to 46% of control reporter activity in SAS- miR-187 cell subclones (Figure 3B). [score:5]
Although there was no significant difference in BARX2 mRNA expression on metastatic or recurrent tumors, a significant decrease in miR-187 expression was seen in tumors with advanced nodal metastasis (N2) relative to contrasting tumors (Figure 7A). [score:5]
Studies have excluded Dab2, FIH suppressors, and other predicted genes as miR-187 targets [7, 17]. [score:5]
The increased cell migration associated with endogenous and exogenous miR-187 expression was decreased by miR-187 inhibition in both SAS (Figure 2G) and OECM1 cells (Figure 2H). [score:5]
To generate reporters for target screening, we cloned sequence fragments of the predicted miR-187 target genes BARX2, BCL6, DYRK2, FAM80B, GRIA3, and HIPK3. [score:5]
miR-187 was shown in our preliminary screening study as the 3rd most conspicuously up-regulated miRNA in HNSCC [7]. [score:4]
Up-regulation of miR-187 was found in 40 (71%) of OSCC tumor tissues. [score:4]
Reporter assays of SAS- miR-187 cell subclone indicated that miR-187 repressed the reporter activity by directly targeting the wild type sequence and that the mutation partially reverted the repression (Figure 3D). [score:4]
Exogenous miR-187 expression did not significantly change the proliferation (Figure 2B, upper) or AIG (Figure 2D, upper) of SAS cells. [score:3]
This study provides novel evidence that BARX2 is a target of miR-187 in OSCC. [score:3]
Establishment of cell subclones with miR-187 or BARX2 expression. [score:3]
Figure 2 miR-187 modulates oncogenicity of OSCC cells(A) miR-187 expression. [score:3]
In addition, cell subclones with exogenous miR-187 and BARX2 expression (designated miR-187/BARX2) were established after viral infection, puromycin selection and fluorescence sorting. [score:3]
In this study, we investigated the oncogenic role of miR-187 by targeting the BARX2 tumor suppressor in OSCC. [score:3]
Dab2 was reported to be a target of miR-187 in ovarian cancers [17]. [score:3]
However, our preliminary Western blot analyses have excluded these genes as miR-187 targets in OSCC cells (Figure 3A). [score:3]
OSCC cell subclones with stable miR-187 expression and controls were established by puromycin selection. [score:3]
Identification of BARX2 as the target gene of miR-187 in OSCC. [score:3]
Increased miR-187 expression was observed in patients with ovarian and gall bladder cancer [18, 19]. [score:3]
miR-187 expression also increases the metastatic rate of xenografic tumors and this is associated with worse host survival. [score:3]
The miR-187 expression in SAS- miR-187 and OECM1- miR-187 subclone increased ~11.2 and ~15.9 folds relative to respective control subclones. [score:3]
The targets and mechanisms associated with miR-187 in OSCC pathogenesis are unknown. [score:3]
BARX2 expression reverted miR-187 -induced cell migration. [score:3]
OECM1 cells expressing BARX2 were treated with miR-187 mimic. [score:3]
Increased miR-187 expression in OSCC tumors and patient plasma. [score:3]
In addition, low miR-187 expression defines the sensitivity of ovarian cancers to taxol therapy [20]. [score:3]
org/) version 6.2 was used to predict the potential targets of miR-187 [7]. [score:3]
miR-187 also represses the tumor-suppressor gene disabled homolog-2 (Dab2) in ovarian cancers [17]. [score:3]
However, studies have also revealed that miR-187 is suppressive to some malignancies, including prostate and pancreatic carcinomas as well as clear renal cell carcinoma [21– 25]. [score:3]
miR-187 targets BARX2 in OSCC. [score:3]
In addition, a significant increase in miR-187 expression was noted in tumors with nodal metastasis relative to tumors without node involvement (Figure 1A). [score:3]
ROC analyses indicated that miR-187 expression in OSCC had a predictive power of 0.68 for distinguishing metastatic from non-metastatic states (Figure 1B). [score:3]
miR-187 expression was not associated with other clinicopathological parameters. [score:3]
Establishment of cell subclones with miR-187 or BARX2 expressionA lentivirus carrying the pre-miR-187 sequence and a red fluorescence (RFP) tag was purchased from Biosetta (San Diego, CA, USA). [score:3]
Exogenous miR-187 expression levels differ between cell lines, which may underlie the differences in its potential to promote proliferation and AIG. [score:3]
To explore the expression of miR-187, 56 OSCC tumors and their paired NCMTs were subjected to (Table S1). [score:3]
Lower, miR-187 mimic treatment does not affect the FIH expression in OSCC cells. [score:3]
However, the oncogenic role of miR-187 and its target gene in OSCC have been unknown. [score:3]
Figure 3 miR-187 targets BARX2 in OSCC(A, E). [score:3]
Overall, miR-187 expression increased the oncogenicity of OSCC cells, especially in the OECM1 cell line. [score:3]
To confirm the targeting of miR-187 on BARX2, HSC3 cells were treated with miR-187 mimic for 48 hr. [score:3]
miR-187 expression increased OSCC oncogenicity. [score:3]
Data showing that miR-187 -induced cell migration was attenuated by BARX2 (Figure 5E) support the notion that miR-187 targeted BARX2 to modulate OSCC cell migration. [score:3]
However, exogenous miR-187 expression significantly increased the migration (Figure 2C, upper) and xenografic tumor growth (Figure 2E) in SAS- miR-187 subclones. [score:3]
Paired t-test; [***] p < 0.01. miR-187 has diverse expression across malignancies and plays differential oncogenic roles in different types of tumors [15, 16, 18– 25]. [score:3]
An miR-187 mimic, miR-187 inhibitor, and scramble (Scr) control were purchased from Applied Biosystems (Foster City, CA, USA). [score:3]
Similarly, the OECM1- miR-187 cell subclone also had lower BARX2 expression (Figure 3G). [score:3]
The TaqMan miRNA assay kit was used to quantify the expression of miR-187, BARX2, and other genes according to the manufacturer's instructions (Applied Biosystems). [score:2]
In addition to its role in oncogenesis, miR-187 takes part in the regulation of inflammation, cell stemness, and insulin secretion [26– 28]. [score:2]
Our findings suggest that in addition to chromosomal deletion, epigenetic regulation by oncogenic miRNAs such as miR-187 is also able to repress BARX2 in OSCC pathogenesis. [score:2]
The survival rate of mice carrying the xenografts of SAS- miR-187 cell subclones was drastically decreased comparing to controls (Figure 6D). [score:1]
Many oncogenic miRNAs are potential serological markers of HNSCC or OSCC [2, 10, 39], and our preliminary analysis further supports that plasma miR-187 is a potential marker of OSCC. [score:1]
The results indicated that the activity of BARX2 reporters was repressed by ~55% in SAS- miR-187 cell subclone relative to control. [score:1]
It would be important to specify the enrichment of these aberrant miRNAs with miR-187 in promoting tumor metastasis in future study. [score:1]
miR-187 modulates oncogenicity of OSCC cells. [score:1]
Functional clues support the oncogenicity of miR-187 in OSCC, particularly with respect to enhancing tumor cell migration. [score:1]
Exogenous BARX2 rescued miR-187-enhanced neck metastasis of SAS cells. [score:1]
Exogenous BARX2 rescued miR-187-enhanced neck metastasis of SAS cellsThe tissue analysis revealed the primary xenografic tumor growth of SAS cell subclones in tongue and the metastatic involvement in neck lymph nodes (Figure 6B). [score:1]
Figure 3C illustrates the complementarity between the BARX2 3′UTR sequence and miR-187. [score:1]
Further study is required to confirm the efficacy of miR-187 as a non-invasive marker of oral premalignant disorders [40]. [score:1]
These subclones were designated SAS- miR-187 and OECM1- miR-187. [score:1]
In addition, the antisense sequence of miR-187 was cloned to generate miR-187asR as a positive control reporter. [score:1]
Therefore, the functional role of miR-187 in different cancers may be paradoxical. [score:1]
The miR-187 gene is located on chromosome 18q12.2. [score:1]
Few studies have investigated the relationship of miR-187 targets to tumorigenesis [7, 17, 24]. [score:1]
ROC analysis indicated that the plasma miR-187 level had a predictive power of 0.77 for distinguishing malignant from non-malignant states (Figure 1D). [score:1]
The proliferation, migration, and AIG in OECM1- miR-187 subclone was higher than control subclone (Figure 2B–2D, lower). [score:1]
A lentivirus carrying the pre-miR-187 sequence and a red fluorescence (RFP) tag was purchased from Biosetta (San Diego, CA, USA). [score:1]
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3
[+] score: 219
Other miRNAs from this paper: hsa-mir-29a
The resulted showed that CD276 mRNA expression was significantly reduced by treatment of miR-187 mimics, and remarkably increased by treatment of miR-187 inhibitor, while the mRNA expression of Dab2 was faintly influenced by these stimulation or inhibition (Figure 4B). [score:9]
Previously, down-regulation of miR-187 predicts a poor prognosis has been reported in clear cell renal cell carcinoma (ccRCC), which demonstrated that down-regulated miR-187 is associated with higher tumor grade and stage, and plays a tumor-suppressive role [21]. [score:9]
MiR-187 mimics, miR mimic control, miR-187 inhibitor, miR inhibitor control, and small interfering RNA targeting CD276 were purchased from GenePharma (Shanghai, China). [score:7]
In ovarian cancer, miR-187 regulates tumor progression through targeting Disabled homolog-2 (Dab2), which resulted in inhibition of epithelial-mesenchymal transition [10]. [score:6]
Indeed, we confirmed that CD276 mRNA and protein were down-regulated by the ectopic expression of miR-187, as showed by Real-time-PCR and, respectively. [score:6]
To demonstrate whether endogenous miR-187 contributes to tumor progression, we transfected SW620 and HT29 cells with miR-187 inhibitor or miR inhibitor control. [score:5]
Over -expression of miR-187 suppressed CRC cell proliferation, migration and invasion, and promoted CRC cell apoptosis. [score:5]
To certify this prediction, we detected the mRNA expression of CD276 and Dab2 in SW620 cells in the presence of miR-187 mimics or miR-187 inhibitor. [score:5]
Kaplan-Meier curve revealed that the overall survival rate and relapse-free survival rate of the low miR-187 expression group was higher than those of the high miR-187 expression group (Figure 1C). [score:5]
To elucidate the expression pattern of miR-187 in CRC, we first detected the expression level of miR-187 in 32 matched CRC tumor and non-tumor tissues by Real-time PCR. [score:5]
Furthermore, we identified CD276 as a direct and functional target of miR-187. [score:4]
In the current study, we revealed significant down-regulation of miR-187 in CRC tissues and cell lines. [score:4]
CD276 is a direct target of miR-187. [score:4]
Therefore, our results suggest that miR-187 may play crucial roles in the development and progression of CRCs by targeting CD276. [score:4]
C. Inhibition of miR-187 with miR-187 inhibitor significantly decreased the invasive potential by Transwell assay (*P < 0.05, **P < 0.01). [score:4]
B. Over -expression of miR-187 inhibited proliferation in SW620 and HT29 cells detected by CCK-8 assays. [score:4]
Recent study showed that miR-187 is significantly down-regulated in many types of human malignancies. [score:4]
Knockdown of miR-187 promotes cell proliferation, invasion and inhibits apoptosis in CRC cells. [score:4]
C. Kaplan-Meier curves for patients grouped based on miR-187 expression; *P < 0.05; **P < 0.01. [score:3]
However, increased expression of miR-187 in ovarian cancer correlated with the better prognostic group, and showed distinct dual roles in cell proliferation and tumor progression of ovarian cancer [10]. [score:3]
In order to explore the mechanisms of miR-187, we identified CD276 as a putative miR-187 target gene. [score:3]
Consistent with the observation in ccRCC, we also demonstrated miR-187 acts as a tumor suppressor in CRC in cell proliferation, apoptosis and invasive capacity. [score:3]
Taken together, these observations indicate that miR-187 inhibits tumor progression of CRC by negatively controlling these cellular phenotypes. [score:3]
Meanwhile, the prognostic value of miR-187 expression was also analyzed in CRC patients. [score:3]
Taken together, these results suggest that miR-187 inhibits tumor growth of CRC in vitro and in vivo. [score:3]
B. The mRNA level of CD276 and Dab2 were detected in the presence of miR-187 mimics or miR-187 inhibitor (**P < 0.01, ***P < 0.001). [score:3]
Restoration of CD276 abolishes the tumor suppressor role of miR-187. [score:3]
As showed, miR-187 expression was relatively low in 3 cell lines (SW1116, SW480 and SW620), while that was relatively high in the other 2 cell lines (LOVO and HT29). [score:3]
B. The mRNA expression level of miR-187 in 80 tumor tissues (T) and 30 non-tumor tissue (N) was detected by Real-time quantitative PCR, *P < 0.05. [score:3]
E. SW620 cells were co -transfected with miR-187 expression vector or the empty vector and CD276 3′-UTR reporter plasmid or its mutant form. [score:3]
In this study, we first measured the expression of miR-187 in CRC tissues and cell lines, and found it was significantly down-regulated compared with corresponding normal controls. [score:3]
These findings suggest the expression pattern functions of miR-187 may be tissue specific. [score:3]
A. The expression level of miR-187 was detected after transfection of mimics. [score:3]
Exogenous miR-187 Agomir increased the level of miR-187 in tumor microenvironment and inhibited the growth of SW620 cells in nude mice (Figure 2F and 2G). [score:3]
As shown in Figure 6B-6D, over -expression of CD276 completely abolished the effects of miR-187 on cell proliferation, apoptosis and invasion in LOVO and HT29 cells. [score:3]
To explore the mechanism by which miR-187 affects the biological functions of CRC cells, we next aimed to investigate the potential gene targets of miR-187 using target prediction programs including, MIRDB and DIANA-MICROT. [score:3]
The miR-187/CD276 axis provides novel insight into the pathogenesis of CRC, and might represent a potential therapeutic target for the treatment of CRC. [score:3]
MiR-187 is down-regulated in CRC and correlated with prognosis of CRC patients. [score:3]
To further confirm whether the tumor-suppressive roles of miR-187 were mediated by CD276, a gain-of-function study was performed. [score:3]
Expectedly, suppression of miR-187 significantly promoted cell proliferation (Figure 3A) and invasion (Figure 3C) of CRC cells. [score:3]
To further confirm this observation, miR-187 expression in another cohort containing 30 normal colorectal tissues and 80 CRC tissues with follow-ups was analyzed. [score:3]
Figure 2 A. The expression level of miR-187 was detected after transfection of mimics. [score:3]
B. Inhibition of miR-187 decreased the caspase-3/7 activity of SW620 and HT29 cells (*P < 0.05, **P < 0.01). [score:3]
Our analysis revealed that CD276 and Dab2 are two potential targets of miR-187. [score:3]
Interesting, CD276, but not Dab2, was negatively correlated miR-187 level in CRC cells (Figure 1D and 4A), indicating CD276 might be the target of miR-187 in CRC. [score:3]
And restoration of CD276 completely abrogated the tumor suppressor role of miR-187. [score:3]
Figure 3 A. Inhibition of miR-187 promoted proliferation in SW620 and HT29 cells detected by CCK-8 assays (**P < 0.01, ***P < 0.001). [score:2]
In summary, the present study provides the essential roles of miR-187 in negatively regulating CRC progression and a novel link between miR-187 and CD276 in CRC. [score:2]
MiR-187 inhibits cell proliferation, migration, invasion and promotes apoptosis in CRC cells. [score:2]
Inversely, knockdown of miR-187 significantly facilitated the malignant phenotype of CRC cells. [score:2]
A. Inhibition of miR-187 promoted proliferation in SW620 and HT29 cells detected by CCK-8 assays (**P < 0.01, ***P < 0.001). [score:2]
Collectively, these data strongly indicate that CD276 is the direct functional mediator of miR-187. [score:2]
Over -expression of miR-187 significantly decreased the invasive potential of SW620 and HT29 cells when transfected with miR-187 mimics compared with control cells (*P < 0.05, **P < 0.01). [score:2]
For example, miR-187 in breast cancer leads to a more aggressive, invasive phenotype and acts as an independent predictor of outcome [9]. [score:1]
The result showed that miR-187 significantly decreased the migratory (Figure 2D) and invasive (Figure 2E) potential of SW620 and HT29 cells. [score:1]
Notably, the highest miR-187 level was detected in NCM460 cells. [score:1]
As demonstrated by, miR-187 decreased the levels of CD276 protein in SW620 and HT29 cells (Figure 4C), which supports our hypothesis to a certain extent. [score:1]
D. The predicted sites of miR-187 binding to the 3′-UTR region of CD276 were detected using bioinformatics prediction tools. [score:1]
Subsequently, we measured the expression levels of miR-187 in 5 CRC cell lines and the normal colonic epithelial cell line NCM460 by Real-time RT-PCR (Figure 1D). [score:1]
H. The mass of the tumors in the group with exogenous miR-187 Agomir was lower than that in the group with exogenous miR-187 Agomir NC, **P < 0.01. [score:1]
Mutant CD276 3′UTR was generated based on the pMIR-CD276-3′UTR by mutating 3 nt that are recognized by miR-187. [score:1]
In this experiment, the nude mice were treated with miR-187 Agomir, which is similar to miR-187 mimics but more stable in vivo [22]. [score:1]
These reporter constructs were used to co-transfect miR-187 mimics cells or control cells. [score:1]
Figure 6LOVO and HT29 cells were transfected with NC mimics or miR-187 mimics together with either pcDNA3.1 or pcDNA3.1-CD276. [score:1]
G. The miR-187 level was detected in tumor tissues upon miR-187 Agomir and Agomir NC treatment (**P < 0.01). [score:1]
LOVO and HT29 cells were transfected with NC mimics or miR-187 mimics together with either pcDNA3.1 or pcDNA3.1-CD276. [score:1]
A. The transcription level of miR-187 in 32 matched CRC tissues (T) and adjacent normal tissues (N) by quantitative real-time PCR and normalized by an endogenous control, U6 RNA, ***P < 0.001. [score:1]
As shown in Figure 1B, miR-187 was significantly decreased in CRC specimens in relative to the normal control. [score:1]
As shown in Figure 4E, the relative luciferase activity of the reporter containing wild-type CD276 3′-UTR was markedly decreased upon miR-187 co-transfection, whereas the luciferase activity of the reporter containing the mutant binding site was unaffected. [score:1]
C. The protein level of CD276 in SW620 and HT29 cells was detected in the presence of miR-187 mimics by. [score:1]
Consistently, elevated caspase-3/7 activity was also observed in miR-187 mimics group (Figure 2C). [score:1]
Meanwhile, similar to the phenotype induced by treatment of miR-187 mimics, silencing of CD276 also decreased migratory ability and invasive potential of LOVO and HT29 cells (Figure 5D and 5E). [score:1]
Using CCK-8 assays, we observed that the growth rate of miR-187 mimics treated cells was inhibited compared with NC mimics -transfected cells (Figure 2B). [score:1]
D. Histograms of the transcription level of miR-187 in human CRC cell lines SW1116, SW480, SW620, HT29 and LOVO, and the normal colonic epithelial cells NCM460; **P < 0.01; **P < 0.001. [score:1]
When the average value of tumor sizes was up to 100 mm [3], the mice were separated into 2 groups randomly, one with subcutaneous injection of miR-187 (Agomir) at different sites, and the other with miR-187 (Agomir) NC. [score:1]
The reporter plasmid was transiently transfected into SW620 cells in the presence of either miR-187 or miR-control. [score:1]
In pancreatic cancer, miR-187 can predict short overall survival (OS) in patients after radical surgery [11]. [score:1]
To verify whether or not that, then, a human CD276 3′UTR fragment containing the wild-type or mutant miR-187 -binding site was inserted downstream of the luciferase open reading frame (Figure 4D). [score:1]
Figure 1 A. The transcription level of miR-187 in 32 matched CRC tissues (T) and adjacent normal tissues (N) by quantitative real-time PCR and normalized by an endogenous control, U6 RNA, ***P < 0.001. [score:1]
To further confirm the role of miR-187 on tumor growth, we performed subcutaneous tumor transplantation experiment (Figure 2F). [score:1]
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[+] score: 37
miRNA gene or target mRNA Species Genome variation Molecular effect PDGFRa Human Mutation 3′UTR Altered miR-140 bindingRattanasopha et al., 2012 miR-140 Human SNP Altered miRNA-140 processingLi et al., 2010, 2011 Zebrafish Overexpression Altred Pdfra repressionEberhart et al., 2008 MSX1 Human SNP 3'UTR Altered miR-3649 bindingMa et al., 2014 FGF2/5/9 Human SNP3'UTR Altered miR-496/miR-145/miR-187 bindingLi D. et al., 2016 miR-17-92 cluster Mouse Homozygous deletion Altered Tbx113, Fgf10, Shox2 & Osr1 repressionWang et al., 2013 miR-200b Mouse Overexpression Altered Smad2, Snail& Zeb112 repressionShin et al., 2012a, b miR-133b Zebrafish Overexpression UnkownDing et al., 2016 MiRNAs are small, 19–23 nucleotide non-coding RNAs that function as post-transcriptional repressors of gene expression, either through messenger RNA (mRNA) degradation or translational repression (Bartel, 2009). [score:14]
miRNA gene or target mRNA Species Genome variation Molecular effect PDGFRa Human Mutation 3′UTR Altered miR-140 bindingRattanasopha et al., 2012 miR-140 Human SNP Altered miRNA-140 processingLi et al., 2010, 2011 Zebrafish Overexpression Altred Pdfra repressionEberhart et al., 2008 MSX1 Human SNP 3'UTR Altered miR-3649 bindingMa et al., 2014 FGF2/5/9 Human SNP3'UTR Altered miR-496/miR-145/miR-187 bindingLi D. et al., 2016 miR-17-92 cluster Mouse Homozygous deletion Altered Tbx113, Fgf10, Shox2 & Osr1 repressionWang et al., 2013 miR-200b Mouse Overexpression Altered Smad2, Snail& Zeb112 repressionShin et al., 2012a, b miR-133b Zebrafish Overexpression UnkownDing et al., 2016 Using microarray analysis, the expression profile of murine miRNAs in the developing lip and PS were analyzed from E10 to E14 (Mukhopadhyay et al., 2010; Warner et al., 2014). [score:12]
miRNA gene or target mRNA Species Genome variation Molecular effect PDGFRa Human Mutation 3′UTR Altered miR-140 bindingRattanasopha et al., 2012 miR-140 Human SNP Altered miRNA-140 processingLi et al., 2010, 2011 Zebrafish Overexpression Altred Pdfra repressionEberhart et al., 2008 MSX1 Human SNP 3'UTR Altered miR-3649 bindingMa et al., 2014 FGF2/5/9 Human SNP3'UTR Altered miR-496/miR-145/miR-187 bindingLi D. et al., 2016 miR-17-92 cluster Mouse Homozygous deletion Altered Tbx113, Fgf10, Shox2 & Osr1 repressionWang et al., 2013 miR-200b Mouse Overexpression Altered Smad2, Snail& Zeb112 repressionShin et al., 2012a, b miR-133b Zebrafish Overexpression UnkownDing et al., 2016 CS, CC, JV: Conception of the work, drafting of the manuscipt, revision of the manuscript, final approval of the manuscript. [score:10]
Similarly, altered miR-496-FGF2, miR-145-FGF5, and miR-187-FGF9 interactions were associated with clefting in 289 nsCLP and 49 nsCPO patients (Li D. et al., 2016). [score:1]
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[+] score: 24
Among early up-regulated miRNAs, miR-187-3p showed the highest up-regulation in our. [score:7]
For the first time, we demonstrated that DOX caused a higher expression of miR-187-3p in human cardiomyocytes. [score:3]
Thus, we may assume that miR-187-3p overexpression in cardiomyocytes is the result of DOX -induced DNA damage. [score:3]
Verified gene targets of miR-187-3p, miR-486-5p, miR-34a, miR-212-3p, miR-34c-3p, miR-675-5p and miR-3911 were not enriched for GO terms related to cardiac and general toxicity responses. [score:3]
Notably, miR-187-3p overexpressing T-lymphoma cells show resistance to DNA damaging agents such as DOX, cisplatin and cyclophosphamide (Yan et al. 2014). [score:3]
However, more studies are needed to unveil the role of miR-187-3p in both cardiotoxicity and the development of heart failure. [score:2]
Validation of miRNA microarray data using qPCR confirmed deregulation of miR-187-3p, miR-182-5p, miR-486-3p, miR-486-5p, miR-34a-3p, miR-4423-3p, miR-34c-3p, miR-34c-5p and miR-1303 in both DOX-Day2 and DOX-Day6 groups. [score:2]
Until now, no reports of miR-187-3p in heart failure and DOX -mediated cardiotoxicity have been observed. [score:1]
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[+] score: 22
Elevated miR-18b expression in human nasopharyngeal carcinoma accelerates cell growth, and knockdown of C-Jun causes a dramatic decrease of miR-18b expression [36]; AP-1 binds to miR-101 promoter and activates its expression where miR-101 can further suppress the c-Fos and subsequently attenuate the AP-1 signaling [37]; miR-187 is expressed at high level in ovarian cancer, and it inhibits the expression of disabled-2 tumor suppressor who can suppress tumorigenicity by reducing c-Fos expression [38, 39]. [score:22]
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7
[+] score: 22
The results reported in Figure 1 confirm the overexpression of miR-483-5p, miR-483-3p, miR-675-5p, miR-21-3p, and the downregulation of miR-187-3p in HMGA1P7 overexpressing MEFs in comparison with the WT ones. [score:8]
Dou C. Liu Z. Xu M. Jia Y. Wang Y. Li Q. Yang W. Zheng X. Tu K. Liu Q. miR-187-3p inhibits the metastasis and epithelial-mesenchymal transition of hepatocellular carcinoma by targeting S100A4Cancer Lett. [score:5]
Finally, in the opposite way, miR-187-3p has been reported as oncosuppressor because of its inhibitory action on metastasis and epithelial-mesenchymal transition of hepatocellular carcinoma and non-small cell lung cancer [38, 39]. [score:5]
Sun C. Li S. Yang C. Xi Y. Wang L. Zhang F. Li D. MicroRNA-187-3p mitigates non-small cell lung cancer (NSCLC) development through down-regulation of BCL6Biochem. [score:4]
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8
[+] score: 20
Other miRNAs from this paper: hsa-mir-155, hsa-mir-296
The downregulation of miR-187-3p expression was associated with advanced HCC TNM stages, metastasis, and poor clinical outcome, while S100A4 was shown to be the direct downstream target of miR-187-3p. [score:9]
HCC cell migration, invasion, and EMT abilities could be inhibited by miR-187-3p overexpression and S100A4 downregulation. [score:8]
Moreover, hypoxia was responsible for the decreased levels of miR-187-3p and an increase in S100A4 expression facilitated HCC metastasis and EMT formation [111]. [score:3]
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[+] score: 20
Non-infected (Fold-change) miRNA [1] (fold change)MX1 myxovirus (influenza virus) resistance 1 [27]Z23168+11.46gga-miR-155(+3.55)gga-miR-206(−2.86)Interleukin 8 (IL8) [28]M16199+11.03gga-miR-32(+7.98)Interferon regulatory factor 7 (IRF7) [29]U20338+2.11gga-miR-142-5p(+2.84)Interleukin1receptor-like1, transcript variant1 [51]AB041738+1.65gga-miR-460 (only expressed in infected lungs)TNF receptor superfamily, member 19 [30]BX931334−1.85gga-miR-187(−4.35)Tipartite motif-containing 7.1 [52]BX934475−1.81NA [2]RAC serine/threonine-protein kinase3 (ATK3) [53]BX950472−1.65NAC-fringe 1 [54] U97157 −1.52 NANote: [1]miRNAs targeting on differentially expressed immune related genes; [2] No miRNAs targeting on the gene; +: Up-regulated with AIV infection; –: Down- regulated with AIV infection. [score:14]
In addition, three down-regulated miRNAs (miR-206, miR-301 and miR-187) also were predicated to target on AIV genome. [score:6]
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10
[+] score: 16
Other miRNAs from this paper: hsa-mir-21, hsa-mir-155, hsa-mir-146b
Overall, these evidences indicate that, through a complex network of miRNAs, IL-10 drives anti-inflammatory responses by upregulating miR146b and miR187 and by downregulating pro-inflammatory miRNAs, such as miR155. [score:7]
6. IL-10 enhances LPS -mediated induction of miR146b and miR187, which post-transcriptionally regulate mRNA encoding for TNF-α and reduce IL-6 and IL-12p40 transcription via inhibition of the transcription factor IkB. [score:4]
On the contrary, upon LPS stimulation, IL-10 rapidly and transiently enhances miR146b and sustains miR187 expression in myeloid cells. [score:3]
miR187 acts as negative modulator of LPS responses by directly limiting TNF-α production at post-transcriptional level and by reducing IL-6 and IL-12p40 transcription via silencing the transcription factor IkB (40) (Figure 1). [score:2]
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11
[+] score: 13
For the latent stage, 18 consistently differentially expressed mature miRNA sequences were identified: 8 were up-regulated (miR-212-3p, miR-21-5p, miR-132-3p, miR-20a-5p, miR-17-5p, miR-27a-3p, miR-23a-3p, miR-146a-5p) and 10 were down-regulated (miR-139-5p, miR-551b-3p, miR-33-5p, miR-708-5p, miR-7a-5p, miR-935, miR-138-5p, miR-187-3p, miR-30e-3p, miR-222-3p) (Table  2). [score:9]
The most common down-regulated miRNAs were miR-30a-5p (6 profiles), followed by miR-139-5p, miR-187-3p, miR-551b-3p, miR-140-3p, miR-324-5p, miR-33-5p, miR-218-5p, miR-378a-3p and miR-29c-5p (Supplementary Table  S4). [score:4]
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12
[+] score: 12
Recent data also demonstrated that miR-187 directly targets TNF-α mRNA and indirectly decreases IL-6 and IL-12p40 expression via down-modulation of IκBζ, a master regulator of the transcription of these latter two cytokines. [score:8]
These results uncover a miRNA -mediated pathway controlling cytokine expression and demonstrate a central role of miR-187 in the physiological regulation of IL-10 -driven anti-inflammatory responses [61]. [score:4]
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13
[+] score: 11
Nevertheless, taking into account only those that were expressed the most upon induction (over 1/100 of average housekeeping genes), we identified miR-187, miR-155, miR-146a, let-7e, miR-29b, miR-34, miR-214, and miR-147 as being substantially upregulated following H. pylori infection. [score:6]
Other miRNAs, which are differentially regulated in H. pylori-activated DCs, deserve further investigation; among them, miR-187, which was strongly upregulated in the H. pylori-activated DCs, could control IL-10 -driven anti-inflammatory responses (Rossato et al., 2012). [score:3]
IL-10 -induced microRNA-187 negatively regulates TNF-alpha, IL-6, and IL-12p40 production in TLR4-stimulated monocytes. [score:2]
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14
[+] score: 8
miR-187 was downregulated in colorectal cancer compared to normal controls, and its decreased expression tendency could also be detected in the plasma of CRC patients compared with healthy control patients. [score:4]
In a similar way, downregulation of miR-187 has been shown in renal cell carcinoma both in tissue and in plasma samples [56]. [score:4]
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15
[+] score: 7
The top 8 downregulated (hsa-miR-200c, hsa-miR-212, hsa-miR-29a, hsa-miR-532, hsa-miR-141, hsa-miR-1, hsa-miR-363, hsa-miR-187) and 8 upregulated (hsa-miR-487, hsa-miR-452, hsa-miR-1233, hsa-miR-92a, hsa-miR-106b, hsa-miR-1290, hsa-miR-320, hsa-miR-26a) miRNAs were presented in Figure 1A. [score:7]
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[+] score: 6
Fru-miR-206-3p, fru-miR-10b-5p, fru-miR-10d-5p, fru-miR-133b-3p, and fru-miR-133-3p exhibited 434, 77, 60, 17, and 15 times higher levels of expression, respectively, in fast muscle compared with cardiac muscle, while fru-miR-144-5p, fru-miR-499-5p, fru-miR-187-3p, fru-miR-499a-5p, and fru-miR-140-3p exhibited 51-, 41-, 37-, 33-, and 17-fold higher expression levels, respectively, in heart muscle compared with fast muscle. [score:3]
Expression levels of fru-miR-196a-5p, fru-miR-206-3p, fru-miR-194-5p, fru-miR-192-5p, and fru-miR-10b-5p in slow muscle were 1305-, 529-, 93-, 85-, and 77-fold higher, respectively, compared with cardiac muscle, while expression levels of fru-miR-187-3p, fru-miR-30e-3p, fru-miR-140-3p, fru-miR-218a-5p, and fru-miR-140-5p were 16-, 16-, 10-, 8-, and 6-fold higher, respectively, in cardiac muscle compared with slow muscle. [score:3]
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[+] score: 6
Seeliger et al. [7] have identified 6 miRNAs upregulated in osteoporotic fracture patients: miR-21, miR-23a, miR-24, miR-25, miR-100 and miR-125b meanwhile Garmilla-Ezquerra et al. [8] detected miR-187 and miR-518f as differentially expressed between sample groups. [score:6]
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[+] score: 6
Although little has been known for the oncogenic role of BCL6 in epithelial malignancies, a recent study reported that microRNA-187-3p inhibited lung cancer development by targeting oncogenic BCL6 [33]. [score:6]
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[+] score: 6
Of the 29 significantly differentially-expressed miRNAs, only 2 were upregulated (miR-21 and miR-187). [score:6]
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20
[+] score: 5
Nevertheless, the 7 SL RNA, as well as Alu sequences, contains many miRNA target sites with small differences from the proper structure but still with a high degree of sequence complementarity to some miRNAs (hsa-miR-187, 151, 210, 217 and 328), i. e. some kind of ‘cryptic’ miRNA target sites. [score:5]
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21
[+] score: 5
MicroRNA-16, miR-125b and miR-187 all reduce TNFα expression by reducing mRNA stability, while miR-181a targets IL-1α mRNA in a similar manner [5– 8]. [score:5]
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[+] score: 4
Several molecules that were differentially up-regulated at 3 and 6 h post- L. major infection, i. e., miR9, miR132, miR-146a, miR-155 and miR-187, are well known to control TLR-receptor signaling in monocytes [27], [50], [51]. [score:4]
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[+] score: 4
MiR-187 is one of the ten most upregulated microRNAs in PTCs, FTCs and PDTCs but apparently remains unaffected in FTAs. [score:3]
This suggests miR-187 as a useful marker for distinguishing FTCs from FTAs that however is not suitable for discriminating FTCs from other carcinomas of follicular origin. [score:1]
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24
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-136, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-139, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-210, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-136, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, mmu-mir-98, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, hsa-mir-452, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-495, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-505, mmu-mir-18b, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-216b, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
Ssc-miR-182, ssc-miR-187, ssc-miR-136, ssc-miR-210, ssc-miR-217 and ssc-miR-10b participate in regulation Neurotrophin signaling pathway by targeting corresponding genes, including BNDF, SHC4, KRAS and FOXO3. [score:4]
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25
[+] score: 4
They assessed the relationship of two miRNAs (miR-182 and miR-187) most differentially expressed in prostate cancer with the clinicopathological characteristics and outcome of patients, and it was observed that miR-187 expression was decreased in advanced prostate cancer cases, which was consistent with microarray data. [score:3]
A subset of six miRNAs (miR-187, miR-18a [*], miR-25, miR-142-3p, miR-140-5p, and miR-204) was capable of correctly classifying bladder urothelial cell carcinoma (UCC) patients with an overall sensitivity of 84.8% and specificity of 86.5% [89]. [score:1]
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26
[+] score: 3
The enzymes of MVA pathway including AACT, HMG-CoA synthase, HMG-CoA reductase and diphosphomevalonate decarboxylase were predicted to be targeted by miR5042-3p, val-miR720; miR477g; miR6196, miR395o-3p, val-miR187; and miR5246, respectively. [score:3]
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27
[+] score: 3
Seven of these miRNAs–miR-509-3p, miR-146a, miR-145, miR-29b-2-star, miR-187, miR-133a, miR-211–were underexpressed in tumors versus controls by at least 6 standard deviations from the mean. [score:3]
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[+] score: 3
These studies had shown that the activation of TIRs and TNF-α receptor results in rapid expression of a host of miRNAs including let-7, miR-9, miR-99b, let-7e, miR-125a, miR-132, miR- 146a, miR-146b, miR-155, miR-187, and miR-223 (Taganov et al., 2006; Tili et al., 2007; Bazzoni et al., 2009; Ceppi et al., 2009). [score:3]
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[+] score: 3
In particular, Bloomston and colleagues [34], using the miRNA microarray chip OSU_CCC v. 3.0, which contains 326 human miRNA probes, identified a subgroup of six miRNAs (miR-30a-3p, miR-105, miR-127, miR-187, miR-452, and miR-518a2) that distinguish long-term survivors with node -positive disease from those succumbing within 24 months. [score:3]
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Origin Tongue Gingiva Tongue [8], [9], [10], [26] HPV status HPV-16 − − − [27] HPV-18 − − + [27] Basal invasive capacity + ++ +++ [9], [28], [29] Genetic background TP53 + + WT [30], [31] CDKN2A (p16) + + + [30], [32], [33] Critical proteins LOX ++ ++ + [9] Tid1 + + − [10] CK1ε ++ + N/A [29] SIRT1 + + N/A [26] Tumor suppressor miRNAs miR-10b +++ + + [27] miR-196a +++ + + [27] miR-491-5p + ++ ++ [34] miR-410 + + N/A [35] miR-99a + + N/A [35] miR-21 + N/A N/A [35] Oncogenic miRNA miR-31 N/A + + [35] miR-146a N/A + + [36] miR-187 N/A + + [37] WT: wild type; N/A: not available. [score:3]
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Moreover, many important components of innate immune system, including IRAK1 and MAPK3, are thought to be targeted by IAV -induced miRNAs (e. g., miR-7, miR-132, miR-146a, miR-187 and miR-1275) [64]. [score:3]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-19a, hsa-mir-21, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-105-1, hsa-mir-105-2, hsa-mir-199a-1, hsa-mir-34a, hsa-mir-199a-2, hsa-mir-205, hsa-mir-214, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-128-1, hsa-mir-141, hsa-mir-144, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-146a, hsa-mir-200c, hsa-mir-128-2, hsa-mir-29c, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-133b, hsa-mir-429, hsa-mir-487a, hsa-mir-515-1, hsa-mir-515-2, hsa-mir-526b, hsa-mir-514a-1, hsa-mir-514a-2, hsa-mir-514a-3, hsa-mir-376a-2, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-656, hsa-mir-542, hsa-mir-378d-2, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-1275, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-2114, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-514b, hsa-mir-378c, hsa-mir-4303, hsa-mir-4309, hsa-mir-4307, hsa-mir-4278, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
For example, the high levels of has-miR-187 promoted lymph node metastasis of breast cancer [26]. [score:1]
Comparing with previous studies of miRNAs, we found that 21 among 31 genes have been reported in previous publications, for example, hsa-miR-105, hsa-miR-187, hsa-miR-214*, hsa-miR-656, and hsa-miR-487a. [score:1]
The miR-187 was increased in breast cancer tissues which could be used as one of the independent prognostic factors and enforced tumor cells invasive ability [26]. [score:1]
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Other miRNAs from this paper: hsa-mir-15a, hsa-mir-16-1, hsa-mir-27b, hsa-mir-206
Recently, Calin et al. identified mutations in six microRNA genes (miR-16-1, miR-27b, miR-29b2/29a, miR122a, miR-187, miR-206) in patients with Chronic Lymphocytic Leukemia (CLL) [5]; none of these mutations were found in a set of 160 individuals without cancer (P <. [score:3]
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However, the involvement of miR-187, miR-299-3p, and miR-628-5p in some aspects of biology, including cancer, has been reported [43]– [46]; thus these miRNAs may play roles in regulating the proliferation of iPS/ES cells. [score:2]
In the case of miR-187, 299-3p, 499-5p, 628-5p, and 888, these miRNAs showed nearly negligible values or were not examined in previous studies [13], [14]. [score:1]
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For instance, miR-187 promotes growth and metastasis of gastric cancer by inhibiting FOXA2 [21]. [score:3]
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[+] score: 2
The predicted structure of pre-miR-342 with the addition of the in del (rs261236356) is shown at rightSeven other miRNAs had local eQTL: miR-146b, miR-181d, miR-187, miR-203, miR-221, miR-322, and miR-503. [score:1]
The predicted structure of pre-miR-342 with the addition of the in del (rs261236356) is shown at right Seven other miRNAs had local eQTL: miR-146b, miR-181d, miR-187, miR-203, miR-221, miR-322, and miR-503. [score:1]
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Several editing events within the seed were found to be much more ancient than previously recognized: editing of miR-27a was found in placental mammals and platypus, thus presumably dating back at least 220 million years, while editing of miR-187*, miR-497 and miR-1251 was shared between placental mammals and marsupials, whose last common ancestor lived 180 million years ago [20]. [score:1]
Human Macaque Mouse Opossum Platypus Chicken Human SNP Opossum SNP Known ValidatedmiR-27a6>1%>1%  >1% No-Human [e]---miR-99b*2 >1%>1%   No-Human [c]-Mouse [c]Mouse [c]miR-140*16   >5% >5%NoNo----miR-187*5  >1%>1%  NoNo----miR-301a20 >1% >5% >5%NoNo----miR-376a-13>1%>1%>1%   No-Human [b,c,d]-Mouse [b,c,d,e,f]Mouse [b,c]miR-376b6>5% >5%   No-Human [b,c,d]-Mouse [b,c,d,f,g]Mouse [b,c]miR-376c6>5% >5%   No-Human [e]-Mouse [b,d,e,f]Mouse [b]miR-3795 >5%>5%   No-Human [a,c,e]-Mouse [c,d,e,f]Mouse [c]miR-3814>5%>5%>5%   No-Human [e]Human [e]Mouse [d,f,g]-miR-4115>5%>5%>5%   No-Human [b,d]-Mouse [c,d,e]Mouse [c]miR-45517 >1%   >1%No-Human [e]Human [e]--miR-4972>5%>5%>5%>5%  NoNoHuman [e]Human [e]Mouse [d,e]-miR-497*20>5%>5%    NoNoMouse [d]---miR-12516 >5%>5%>1%  NoNoMouse [d,e]-                     - -Summary of the output from the miRNA editing detection pipeline, run with a 5% or 1% frequency cutoff. [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-30a, hsa-mir-31, hsa-mir-98, hsa-mir-99a, hsa-mir-101-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-197, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-211, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-138-1, hsa-mir-146a, hsa-mir-200c, hsa-mir-155, hsa-mir-128-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-375, hsa-mir-328, hsa-mir-337, hsa-mir-338, hsa-mir-339, hsa-mir-384, hsa-mir-424, hsa-mir-429, hsa-mir-449a, hsa-mir-485, hsa-mir-146b, hsa-mir-494, hsa-mir-497, hsa-mir-498, hsa-mir-520a, hsa-mir-518f, hsa-mir-499a, hsa-mir-509-1, hsa-mir-574, hsa-mir-582, hsa-mir-606, hsa-mir-629, hsa-mir-449b, hsa-mir-449c, hsa-mir-509-2, hsa-mir-874, hsa-mir-744, hsa-mir-208b, hsa-mir-509-3, hsa-mir-1246, hsa-mir-1248, hsa-mir-219b, hsa-mir-203b, hsa-mir-499b
Analysis of patients with asthma and allergic rhinitis showed further alterations in expression for six miRNAs: miR-224, miR-498, miR-187, miR-874, miR-143, miR-886-3p as compared to the control subjects. [score:2]
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[+] score: 2
MicroRNAs miR-187 (previously identified to be induced by influenza A virus [26]), miR-147b, miR-190b, miR-874, and the miR-449 family (miR-449a, miR-449b, and miR-449c) were all validated as highly regulated by influenza A virus infection (Figure 2). [score:2]
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[+] score: 1
Casanova-Salas I. Rubio-Briones J. Calatrava A. Mancarella C. Masiá E. Casanova J. Fernández-Serra A. Rubio L. Ramírez-Backhaus M. Armiñán A. Identification of miR-187 and miR-182 as biomarkers of early diagnosis and prognosis in patients with prostate cancer treated with radical prostatectomyJ. [score:1]
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[+] score: 1
Among the DEMs that were common to BEAS-AKT1-E17K, BEAS-PIK3CA-E545K and BEAS-shPTEN cells miR-203, miR-196a and miR-187 showed the highest fold changes. [score:1]
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[+] score: 1
2 −2.40(52) hsa-miR-127-5p 14q32.2 −2.35(12, 29) hsa-miR-127-3p 14q32.2 −2.35(52, 59) hsa-miR-411* 14q32.2 −2.30 hsa-miR-125b-1* 11q24.1/21q21.1 −2.27 hsa-miR-411 14q32.2 −2.23(29) hsa-miR-379 14q32.2 −2.22(29, 52) hsa-miR-431* 14q32.2 −2.22 hsa-miR-767-5p Xq28 −2.20 hsa-miR-139-3p 11q13.4 −2.17 hsa-miR-154 14q32.2 −2.16(12) hsa-miR-1224-5p 3q27.2 −2.15 hsa-miR-187 18q12.1 −2.14(12) hsa-miR-95 4p16.1 −2.10(14) hsa-miR-369-5p 14q32.2 −2.05 hsa-miR-665 14q32.2 −2.05 hsa-miR-494 14q32. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7e, hsa-mir-147a, hsa-mir-125a, hsa-mir-99b, hsa-mir-147b
When applying SVM classifier on the set TE-C, 28 out of the 30 human pre-miRNAs are correctly recognized (the missed ones are "hsa-mir-147" and " hsa-mir-187") and 881 out of the 1000 pseudo-miRNAs are detected as negative, which gives a sensitivity of 93.3% and specificity of 88.1% (Table 1). [score:1]
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Casanova-Salas I Rubio-Briones J Calatrava A Mancarella C Masiá E Casanova J Identification of miR-187 and miR-182 as biomarkers of early diagnosis and prognosis in patients with prostate cancer treated with radical prostatectomyJ Urol. [score:1]
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Levels of 15 miRNAs: miR-223, miR-1290, miR-4725-3p, miR-4793-3p, miR-410, miR-187, miR-375, miR-203, miR-200b-5p, miR-194-3p, miR-200a, miR-215, miR-31, miR-192-3p and miR-141 were significantly different between NEC and SIP tissues (0.12–59.05 fold; Table 2). [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-21, hsa-mir-23a, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-192, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-221, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-152, hsa-mir-125b-2, hsa-mir-146a, hsa-mir-193a, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-148b, hsa-mir-193b, hsa-mir-181d, hsa-mir-92b, hsa-mir-454, ssa-mir-10a-1, ssa-mir-10a-2, ssa-mir-10b-1, ssa-mir-10b-2, ssa-mir-10b-3, ssa-mir-10b-4, ssa-mir-10d-1, ssa-mir-10d-2, ssa-mir-122-1, ssa-mir-122-2, ssa-mir-125b-1, ssa-mir-125b-2, ssa-mir-125b-3, ssa-mir-146a-1, ssa-mir-146a-2, ssa-mir-146a-3, ssa-mir-148a, ssa-mir-148b, ssa-mir-152, ssa-mir-16a-1, ssa-mir-16a-2, ssa-mir-181a-1, ssa-mir-181a-2, ssa-mir-181a-3, ssa-mir-181a-4, ssa-mir-181a-5, ssa-mir-181b, ssa-mir-181c, ssa-mir-192a-1, ssa-mir-192a-2, ssa-mir-192b, ssa-mir-193, ssa-mir-21a-1, ssa-mir-21a-2, ssa-mir-21b, ssa-mir-221, ssa-mir-23a-3, ssa-mir-23a-4, ssa-mir-23a-1, ssa-mir-23a-2, ssa-mir-25-1, ssa-mir-25-2, ssa-mir-25-3, ssa-mir-26a-1, ssa-mir-26a-2, ssa-mir-26a-3, ssa-mir-26a-4, ssa-mir-26a-5, ssa-mir-26a-6, ssa-mir-26b, ssa-mir-26d, ssa-mir-30a-3, ssa-mir-30a-4, ssa-mir-30a-1, ssa-mir-30a-2, ssa-mir-30b, ssa-mir-30c-1, ssa-mir-30c-2, ssa-mir-30d-1, ssa-mir-30d-2, ssa-mir-30e-1, ssa-mir-30e-2, ssa-mir-30e-3, ssa-mir-454, ssa-mir-462a, ssa-mir-92a-1, ssa-mir-92a-2, ssa-mir-92a-3, ssa-mir-92a-4, ssa-mir-92b
In contrast, some other miRNAs listed in the Table 1 have been reported as oncogenes, e. g. MiR187 [68], MiR193 [69], or MiR454 [70]. [score:1]
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[+] score: 1
miR-187, miR-202, and miR-299-3p were not significantly correlated with any of the four markers. [score:1]
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[+] score: 1
Casanova-Salas I. Rubio-Briones J. Calatrava A. Mancarella C. Masia E. Casanova J. Fernandez-Serra A. Rubio L. Ramirez-Backhaus M. Arminan A. Identification of miR-187 and miR-182 as biomarkers of early diagnosis and prognosis in patients with prostate cancer treated with radical prostatectomyJ. [score:1]
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[+] score: 1
However, after validating these 7 miRNA in an independent set of samples, miR-187*, miR-371-5p, and miR-378 remained significantly associated with gastric cancer serum samples (Liu et al., 2012a). [score:1]
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The LPS -induced microRNA signature was formed by a large cluster of miRs, including miR-155 and miR-187, as can be seen in the third panel, Figure 1A. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7d, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-30a, hsa-mir-32, hsa-mir-33a, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-147a, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-200b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-138-2, hsa-mir-142, hsa-mir-144, hsa-mir-125b-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-190a, hsa-mir-200c, hsa-mir-155, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-365b, hsa-mir-328, gga-mir-33-1, gga-mir-125b-2, gga-mir-155, gga-mir-17, gga-mir-148a, gga-mir-138-1, gga-mir-187, gga-mir-32, gga-mir-30d, gga-mir-30b, gga-mir-30a, gga-mir-30c-2, gga-mir-190a, gga-mir-204-2, gga-mir-138-2, gga-let-7d, gga-let-7f, gga-mir-146a, gga-mir-205b, gga-mir-200a, gga-mir-200b, gga-mir-34a, gga-mir-30e, gga-mir-30c-1, gga-mir-205a, gga-mir-204-1, gga-mir-23b, gga-mir-142, hsa-mir-449a, hsa-mir-489, hsa-mir-146b, hsa-mir-548a-1, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-33b, hsa-mir-449b, gga-mir-146b, gga-mir-147, gga-mir-489, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-144, gga-mir-460a, hsa-mir-147b, hsa-mir-190b, gga-mir-22, gga-mir-460b, gga-mir-1662, gga-mir-1684a, gga-mir-449c, gga-mir-146c, gga-mir-449b, gga-mir-2954, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, gga-mir-365b, gga-mir-33-2, gga-mir-125b-1, gga-mir-190b, gga-mir-449d, gga-mir-205c
To validate the present results of miRNA-sequencing, miR-30E-3P, miR-187-3P, miR-1662, and miR-147 these four miRNAs were selected from all miRNAs identified in this study for qRT-PCR validation. [score:1]
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[+] score: 1
Interestingly, more positively correlated microRNA-mRNA pairs than negatively correlated pairs were observed for all microRNAs with the exception of nine, miR-181B2, miR-582, miR-497, miR-559, miR-561, miR-101-1, miR-187, miR-572 and miR-301A (Figure 5). [score:1]
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